The proposed work continues a long-term study of radiation-induced mutagenesis in the bacterium E. coli. It has been determined that ultraviolet light (UV), like many other mutagenic and carcinogenic agents, acts as a regulatory signal by damaging DNA and/or interrupting DNA replication. The exposure to UV radiation causes normal E. coli cells to derepress a number of functions that are ordinarily kept under repression, including an error-prone type of DNA repair activity "SOS repair" that is responsible for UV mutagenesis. We are primarily interested in the regulation of SOS repair activity, and especially in elucidating the roles of the recA, lexA and Sfi genes in control of the coordinated expression of SOS repair and other inducible SOS functions. We propose to map Sfi mutations, which we believe to affect the activity of one or more proteolytic enzymes, directly or indirectly, and to demonstrate their ability to alter the stability of puromycin fragments and other polypeptides that are usually subject to rapid degradation. The biochemical and genetic analysis of Sfi mutations will be accompanied by continuing efforts to understand their role in "fine-tuning" the expression of the inducible functions activated by DNA damage.